In a normal human heart, the sinus node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker initiating rhythmic electrical excitation of the heart chambers. A cardiac impulse arising from the sinus node is conducted to the atrial chambers, causing a depolarization known as a P-wave and a corresponding contraction of the atrial chambers. The excitation pulse is further transmitted to and through the ventricles via the atrioventricular (A-V) node and a ventricular conduction system causing a depolarization known as an R-wave and a corresponding contraction of the ventricular chambers.
Disruption of this natural pace-making and conduction system as a result of aging or disease can be successfully treated by artificial cardiac pacing using implantable cardiac stimulation devices, including pacemakers and implantable defibrillators, which deliver rhythmic electrical pulses or anti-arrhythmia therapies to the heart at a desired energy and rate. Stimulation may be delivered to the atrial and/or the ventricular heart chambers depending on the location and severity of the conduction disorder.
In a dual chamber, demand-type pacemaker, commonly referred to as DDD pacemaker, an atrial channel and a ventricular channel each include a sense amplifier to detect cardiac activity in the respective chamber and an output circuit for delivering stimulation pulses to the respective chamber. If the atrial channel does not detect an intrinsic atrial depolarization signal (a P-wave), a stimulating pulse will be delivered to depolarize the atrium and cause contraction. Following either a detected P-wave or an atrial pacing pulse, the ventricular channel attempts to detect a depolarization signal in the ventricle. If no R-wave is detected within a defined atrial-ventricular interval (AV interval or delay), a stimulation pulse is delivered to the ventricle to cause a ventricular contraction. In this way, atrial-ventricular synchrony is maintained by coordinating the delivery of ventricular output in response to a sensed or paced atrial event.
In dual chamber stimulation devices, therefore, accurate sensing of evoked responses and the intrinsic deflection of the naturally occurring cardiac events, also referred to as “intrinsic” events, is crucial for achieving atrial-ventricular synchrony and for other desired functions, such as mode switching and the like. Therefore, atrial undersensing, i.e., the failure to sense intrinsic atrial depolarization signals can seriously compromise atrial-ventricular synchrony. Atrial undersensing may arise from a number of different sources, including, by way of example, the patient's activity level, atrial lead dislodgment, improper atrial sensitivity setting, or variations in P-wave amplitude induced by respiration.
While many techniques have been incorporated into dual chamber pacemaker technology to improved atrial sensing reliability, the occurrence of undersensing remains a problem that continues to compromise the performance of many implanted device. For example, atrial fibrillation is often not detected as a result of undersensing intrinsic activity in the atrium. Failing to detect atrial fibrillation typically does not cause discomfort for the patient because the high rate atrial tachycardia is not tracked and the pacemaker does not go to the maximum track rate and thus overdrive the ventricle at an elevated rate. However atrial fibrillation is a serious problem and can result in stroke if not recognized or treated with anticoagulant drugs.